Veterinary World, Vol.

1(10): 296-298 RESEARCH

Prevalence and Haemato-Biochemical Studies of

Gastro-intestinal Parasites of Indian Elephants
(Elephas maximus)
R.G.Jani

Coordinator, Wildlife Health

Department of Veterinary Medicine, Veterinary College, G.A.U., Anand. Gujarat

Abstract
Faecal samples were collected from 40 Indian elephants (Elephas maximus) revealed 62.5 percent
parasitic prevalence. Amongst the single infection of parasites, high prevalence of Fasciolias spp. (15.00
%) was observed followed by percent prevalence of mixed infection. Elephants harbouring parasites
were found clinically dull, depressed and lethargic. About 48 percent elephants manifested dehydration
and loose faeces grossly along with a habit of soil licking. The haematological studies of elephants
harbouring parasites revealed mild anaemia and eosinophilia where as biochemical studies revealed
non-significant hypoproteinemia on comparison with elephants that were not harbouring parasites.
Keywords: Elephant, prevalence, haematological, biochemical.

Introduction either single or mixed species of parasitic ova where

Apar t from free-living population of Indian
elephants (Elephas maximus) found in several
protected areas, domesticated and trained elephants
are being used for drought pur pose by forest
department, in circus and in temples for religious
occasions in India. Several parasitic diseases invariably
affect health status of the elephants as like in other
domesticated animals. The manifestation of illness of
working elephants many a times is ignored on account
of lack of awareness. Therefore, an attempt was made
in present study to know the prevalence rate of
parasites and to evaluate any alteration in
haematological and biochemical variation if any.
Material and Methods
Total 40 elephants that were kept in different
temples of Gujarat were screened for their health status.
The faecal and blood samples were collected and
examined in laboratory as per the standard method
described by Sloss and Kemp (1978) as well as by
Schalm et al. (1975). The biochemical estimations were
analysed by using the diagnostic kits supplied by Span
Diagnostic Pvt. Ltd., Surat-7, India.
Result
In the present study, all together forty elephants
were screened for the prevalence of parasitic infection.
Faecal samples from the 25 (62.5%) elephants revealed
as 15 (37.5%) samples revealed no parasitic ova. The
result of the faecal sample examination is presented
in table-1. The over all prevalence of parasitic infection
was found as 62.5 per cent. The clinical examination
of infected elephant revealed dullness, lachrymation,
depression and mild dehydration with semi loose faeces
in 12 (48 %) elephants along with the vices of soil
licking. The haematological and biochemical
parameters of parasitic affected elephants were
compared with that other healthy elephant is presented
in table -2.
Non significant low level of haemoglobin, total
erythrocyte count and packed cell volume were found
in elephants harbouring the parasites. Where as a
significant (P<0.05) eosinophilia was recorded in the
elephants harbouring the parasites in the present study.
No significant biochemical alteration was observed
except non-significant low serum protein level in
elephants harbouring the parasites.
Discussion
The study was attempted to know the prevalence
of parasitic species of the Indian elephants as well as
to understand their impact on the body with reference
to haematological and biochemical parameters. In the
present study, over all prevalence of parasitic infection
was recorded as 62.5 per cent. The single parasitic
prevalence was found as 60 per cent where as mixed

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 Prevalence and Haemato-Biochemical Studies of Gastro-intestinal Parasites of Indian Elephants

Table-1: Checklist of parasitic ova observed from the elephants.

Parasitic spp. ova Number of infected elephants Over all prevalence
(n=25)(Species specific prevalence %) (Percent)
Fasciolia spp. 06 (24.00) 15.00
Paramphistosomum spp. 04 (16.00) 10.00
Strongyloides spp. 02 (08.00) 05.00
Oesophagostomum spp. 02 (08.00) 05.00
Murshidia spp. 01 (04.00) 02.50
Ascaria spp. 01 (04.00) 02.50
Paramphistomum spp. and Fasciolia spp. 03 (12.00) 07.50
Ascaria spp. and Paramphistosomum spp. 02 (08.00) 05.00
Fasciolia spp. and Strongyloides spp. 02 (08.00) 05.00
Fasciolia sp. and Ascaria spp. 01 (04.00) 02.50
Fasciolia spp., Strongyloides spp. and Ascaria spp. 01 (08.00) 02.50
Normal 15 -
Total 25 62.50

infection was recorded as 40 per cent. The higher
prevalence of Fasciolia spp. (15.00 %) was recorded
in the present study followed by Paramphistosomum
spp. (10.00 %), Strongyloides spp . (05.00 %),
Oesophagostomum spp. (05.00 %) and Ascaria spp.
(02.50 %). Dutta and Bordoloi (1989) recorded 23.33
per cent prevalence of Fasciolia spp. from elephants
of Manas area, Assam. The high prevalence of fasciolia
spp. amongst the different parasites in the present study
might be due to the preference of the elephants for
water bodies and habit of soil licking. The prevalence
of various helminthic parasites of elephants has been
documented by several workers from the different parts
of India (Deka et al., 1985, Rao et al., 1990, Tripathi et
al., 1997). Apart from this the migration of elephants
from one place to other for draught purpose and for
other ceremony work could have favoured the mixed
parasitic infection with clinical signs of dullness and
depression.
Haematological findings of affected elephants
with non-significant low haemoglobin, packed cell
volume and total erythrocyte count suggested anaemic
condition on comparison with healthy elephants, which
substantiate the findings of anaemia by Sarode et al.
(1991). The observed significant eosinophilia in affected
group attributed to reflection of hypersensitivity to
parasites (Coles, 1986). No biochemical alteration was
recorded in elephants harbouring the parasites
however, non-significant low serum total protein values
were recorded in the present study. Hypo proteinaemia
due to parasitic infection in different species have been
documented. (Ross and Todd, 1965, Soulsby, 1982).

Table-2: Comparison of Haematological and Biochemical Parameters in parasite harbouring and

in healthy elephants.

Parameters Affected group (n=25) Control group (n=15)

Haemoglobin (g/dl) 8.96+ 0.43* 11.25+ 0.78
Total erythrocyte counts (TEC)(X106/cu.mm.) 2.42 + 0.25* 2.64 + 0.06
Total Leucocyte count (TLC) (X103/cu.mm.) 6.66 + 0.46 6.90 + 0.18
Packed Cell Volume (%) 24.41+ 1.32* 37.67+ 0.80
Neutrophil(%) 65.00+ 8.02 32.00+ 1.38
Lymphocyte(%) 27.62 + 8.05 61.17 + 1.58
Eosinophil (%) 16.16 + 2.15* 03.50 +0.37
Monocyte(%) 02.02 + 0.21 03.24 + 0.86
Basophil (%) - -
Total Protein(g/dl) 08.13+ 1.12* 09.05 + 0.31
Cholesterol (mg/dl) 39.16+ 1.87 42.50+ 1.65
Blood urea Nitrogen (mg/%) 12.10 + 0.34 13.65 + 0.49
Blood Glucose(mg%) 59.28 + 17.76 61.64+ 10.25

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 Prevalence and Haemato-Biochemical Studies of Gastro-intestinal Parasites of Indian Elephants

Acknowledgement Print 4: 10: 23.

Author is thankful to Dr.Ramesh Sabapara,
Veterinary officer, Vadodara, The Dean, Veterinary
College, Anand and Mahants of Temples for providing
the facilities for doing the study work and staff of the
Kankaria zoo and of temple for their co-operation and
support.
References
1. Coles, E. H. (1986): Veterinary Clinical
Pathology. 4 th Edn. W.B.Saundrs Company,
Philadelphia.
2. Deka, D.C., Baruah, D.K., Barkakoti, M.K. and
Lahkar, B .C.(1985):Proceeding of the
workshop on wildlife health for veterinarian.
Wildlife Institute of India, Dehradun.
3. Dutta, G.C. and Bordoloi, G.C. (1989): Zoo
4. Rao, K.N.P., Bandhopadhyay, A.C. and Gopal,
R.(1990): Zoo Print. 5: 10: 18.
5. Ross, J.G. and Todd, J.R.(1965): Br.Vet. J.
121:55-64.
6. Sarode, D.B., Hatwar, A.K. and Hiwase, S.D.
(1991): Zoo Print 6: 11: 10-11.
7. Schalm, O.W., Jain, N.C. and Carroll, E.J.
(1975): Veterinary Haematology.3 rd Edn. Lea
and Febiger, Philadelphia, USA.
8. Sloss, M.W. and Kemp, R.L. (1978): Veterinary
Clinical Parasitology. 5th Edn. Iowa State
University Press, Ames, Iowa, USA.
9. Soulsby, E.J.L.(1982): Helminths, Arthropods
and Protozoa of Domesticated Animals. 7th
Edn. Baillere and Tindall, London.
10. Tripathi, S.B., Acharjyo, L.N. and Parhi, N.K.
(1997): Indian J.Vet.Med.17, 1: 48-49.

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Test tube experiments may help identify the most hazardous prion proteins
Mixing up normal and infectious prions in test tubes can generate entirely new forms of infectious prion.
Infectious prion proteins from hamsters can change normal proteins from mice into new, infectious forms of prion -
simply by mixing the proteins together in a test tube. Researchers at the University of Texas Medical Branch in
Galveston suggest their discovery could be turned into a useful test for whether a given prion strain is transmissible
from one species to another. Prion proteins are responsible for Creutzfeld-Jakob disease and “mad cow” disease. But
they also found that when a prion jumps species, it produces a new kind of prion. “This is very worrisome,” says
Claudio Soto, who led the research, published in Cell. “The universe of possible prions could be much larger than we
thought.” Normal prion protein, or PrP, is found throughout the body but is concentrated in the brain. Its exact role
is not known, although it has been linked to cell signalling, metal-ion transport, and blood-cell manufacture. The
protein can adopt malformed shapes that cause disease. Those proteins, which are resistant to degradation, bind
and convert normal protein to their troublesome conformation. Over time, the diseased protein builds up and forms
fibrils in the brain, causing neurodegeneration and ultimately death.
Generally, prions are limited to a specific host and a few related species. But prions sometimes cross the
species barrier to infect new hosts. Notably, prions from cows have hopped to humans, causing disease in 208
people, mostly in the UK. Now, scientists wonder if the prion-induced chronic wasting disease (CWD), which afflicts
elk and deer in the US, could jump to humans. Since prion diseases have long dormant periods, the fact that there
are no human cases of CWD doesn’t necessarily indicate that people won’t develop symptoms in the future. “At this
point, we cannot predict the species barrier just by looking at the sequence” of the prion protein, Soto says. But his
laboratory has developed a test-tube method, analogous to the polymerase chain reaction for DNA, to amplify
prions. Their protein misfolding cyclic amplification (PMCA) protocol starts with a minute amount of prion protein and
an excess of normal PrP from healthy brain extract. Over repeated cycles of incubation (allowing the proteins to
interact) and sonication (to break those interactions and allow the malformed prions to access other normal protein),
the process makes more and more infectious protein.
In the current study, Soto and his colleagues show that the technique allows hamster prions to convert
mouse proteins, and vice versa. Although prion infections can pass between hamsters and mice in vivo, the process
takes years and only some animals develop disease. “Here, we crossed the barrier between hamsters and mice in a
couple of weeks in vitro,” Soto says. “In our technology, it’s actually more efficient than real life.” “It is exciting and
interesting that a well-characterized, naturally occurring species barrier to prion infection can be breached without
mutation of the PrP sequence,” says biochemist Surachai Supattapone, who researches prions at Dartmouth Medical
School in Hanover, New Hampshire, and was not involved in the study. “It is also interesting that the newly produced
prions display novel strain properties, because this observation is consistent with the idea that naturally occurring
prion strains might arise as a result of cross-species transmission.” Whereas PrP has one healthy conformation, there
are multiple possible shapes that cause health problems. In the study, the new prions caused disease within different
time frames, affected different areas of the brain, and showed different resistance to protein-digesting enzymes
compared with the original strains. This suggests that new kinds of prion, with potentially differing characteristics,
can be born every time a misfolded prion protein lands in a new species.

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